THE SCROTUM AND TESTIS

SCROTAL WALL

The testicles are maintained in position within the scrotal cavity by the structures of the spermatic cord. Each testicle and spermatic cord is invested in six distinct tissue layers that are acquired as a result of the descent of the gonads from the retroperitoneum into the scrotum during fetal life.

From superficial to deep, the first layer is the scrotal skin, thin in texture, brownish in appearance and highly distensible. It generally assumes a rugated pattern and is continuous with the skin of the mons pubis and penis superiorly, the perineum posteriorly, and the medial thighs laterally. Unlike these adjacent areas, the scrotal skin contains abundant sebaceous follicles, sweat glands, sparsely distributed hair, and a distinct median raphe that corresponds to the scrotal septum within the scrotum and is continuous with the median raphé of the perineum.

Beneath the scrotal epithelium is a thin, fibrous, netlike and highly vascular tissue layer that contains elastic and smooth muscle fibers, and is termed the tunica dartos (dartos = “flayed”). This is the superficial fascia of the scrotum (Colles fascia) that has been previously described (see Plate 2-2 ). It is a continuation of Scarpa fascia of the abdomen and Colles fascia of the urogenital triangle in the perineum (see Plates 2-2 and 2-3 ). The connective tissue from this layer extends inward to form the scrotal septum, which divides the scrotum into a compartment for each testicle.

Deep to the dartos fascia and separated from it by loose areolar tissue is the external spermatic fascia, a continuation of the external oblique fascia of the abdominal wall. Beneath the external spermatic fascia is the cremasteric fascia, which is composed of a double layer of areolar and elastic tissue that encloses a thin layer of striated muscle. The cremasteric fascia is a continuation of the internal oblique fascia and occasionally contains a few fibers from the transversus abdominus muscle. It is the cremasteric fascia that is responsible for the retraction of the testicles, protecting them from trauma and stimuli such as cold through the cremasteric reflex. This reflex is necessary for thermoregulatory control, as it maintains the testicles at the optimal temperature for spermatogenesis.

Deep to the cremasteric fascia is the internal spermatic fascia that closely invests the testicles and inner cord structures. This layer of loose connective tissue is a continuation of the transversalis fascia that lines the abdominal and pelvic cavities.

Beneath the internal spermatic fascia lies the tunica vaginalis. During development, the peritoneum forms two layers that cover each testis as it descends, one anteriorly and one posteriorly. The posterior peritoneum forms the visceral tunica vaginalis that surrounds the testicle where it is closely adherent to the tunica albuginea of the testicle. The outer, parietal layer of the tunica vaginalis is derived from the peritoneum of the anterior abdomen and is adherent to the overlying internal spermatic fascia. It is separated from the visceral layer by endothelial cells that form a small, fluid-filled space between it and the visceral layer. It is within this potential space that hydroceles form.

Within the spermatic cord, running along with the vas deferens, is the inferior spermatic nerve, derived from the pelvic plexus and carrying sympathetic and parasympathetic nerve fibers. It is believed that this nerve is the main neural regulator of testosterone secretion in the testis.

Two remnants from fetal development may be present in the adult scrotum and lie beneath the visceral layer of the tunica vaginalis: (1) the appendix testis (hydatid of Morgagni) on the upper pole of the testis and (2) the appendix epididymis (paradidymis), attached to the head (globus major) of the epididymis. The appendix testis represents remnants of the fallopian tube and is derived from the cranial end of the primitive müllerian duct, whereas the appendix epididymis is a vestige of the cranial end of the mesonephric duct (see Plate 1-2 ).

BLOOD SUPPLY OF THE TESTIS

The arterial supply to the testis is derived from three sources: the internal spermatic artery, the deferential (vasal) artery, and the external spermatic or cremasteric artery. The internal spermatic artery originates from the abdominal aorta just below the renal artery. Embryologically, the testicles lie opposite the second lumbar vertebra and keep the blood supply acquired during fetal life. The internal spermatic artery joins the spermatic cord above the internal inguinal ring and pursues a course adjacent to the pampiniform venous plexus to the mediastinum of the testicle. The vascular arrangement within the pampiniform plexus, with the counter-flowing artery and veins, facilitates the exchange of heat and small molecules. For example, testosterone passively diffuses from the veins to the artery in a concentration-limited manner, and a loss of the temperature differential created by this system is associated with testicular dysfunction in men with varicocele and cryptorchidism.

Near the mediastinal testis, the internal spermatic artery is highly coiled and branches before entering the testis. Extensive interconnections between the internal spermatic and deferential arteries allow maintenance of testis viability even after division of the internal spermatic artery. The testicular arteries penetrate the tunica albuginea and travel inferiorly along the posterior surface of the testis within the parenchyma. Branching arteries pass anteriorly over the testicular parenchyma. Individual arteries to the seminiferous tubules, termed centrifugal arteries, travel within the septa that contain tubules. Centrifugal artery branches give rise to arterioles that supply individual intertubular and peritubular capillaries.

The deferential artery (artery of the vas) may originate from either the inferior or superior vesical artery (see Plate 2-6 ) and supplies the vas deferens and the cauda epididymis. A third artery, the external spermatic or cremasteric artery, arises from the inferior epigastric artery inside the internal inguinal ring, where it enters the spermatic cord. This artery forms a network over the tunica vaginalis and usually anastomoses with other arteries at the testicular mediastinum.

Veins within the testis are unusual in that they do not run with the corresponding intratesticular arteries. Small parenchymal veins empty into either the veins on the testis surface or into a group of veins near the mediastinum testis. These two sets of veins join with deferential veins to form the pampiniform plexus. The pampiniform plexus consists of branches of freely anastomosing veins from (1) the anterior (or internal) spermatic veins that emerge from the testicle and accompany the spermatic artery to enter the vena cava; (2) the middle deferential group that accompanies the vas deferens to pelvic veins; and (3) the posterior or external spermatic group that follows a course along the posterior spermatic cord. The latter group empties into branches of the superficial and deep inferior epigastric veins and the superficial and deep pudendal veins. The middle and posterior veins provide collateral venous return of blood from the testicles after internal spermatic vein ligation with varicocelectomy.

The right internal spermatic vein enters the inferior vena cava obliquely below the right renal vein forming a natural “valve” to reduce retrograde blood flow, whereas the left vein terminates in the left renal vein at right angles, without a natural valve. This anatomic relationship is thought to explain the fact that 90% of varicoceles are on the left side.

With varicocele formation, the blood flow in the internal spermatic vein is reversed, thus disturbing venous drainage from the testis and potentially elevating scrotal temperature. As a consequence, orchalgia and infertility can occur. In high-ligation varicocelectomy procedures (Palomo), the internal spermatic artery and vein are both ligated above where the deferential vessels and the external spermatic veins exit the spermatic cord, thus affording sufficient collateral circulation to maintain testis viability. During inguinal or subinguinal procedures, care is needed to spare the internal spermatic artery, as collateralization may be less extensive at this anatomic level.

TESTIS, EPIDIDYMIS, AND VAS DEFERENS

The testicle is encased within a thick, fibrous capsule known as the tunica albuginea. The tunica is covered by the closely adherent, glistening peritoneum (tunica vaginalis). Multiple septa from the capsule divide the interior of the testicle into several dozen pyramid-shaped lobules. The testis shows ethnic variations in size, but is normally 4 cm in length and 3 cm in diameter (18 to 20 mL in volume).

Within each testicle, each lobule contains one or several tortuous seminiferous tubules which, when uncoiled, measure 1 to 2 ft in length. These tubules converge at the testicular hilum (mediastinum testis), where they straighten and anastomose to form the rete testis. The rete testis tubules empty into 8 to 10 efferent ducts (ductuli efferentes) that carry sperm to the caput epididymis. Occasionally a blind-ending efferent duct is observed (vas aberrans). Spermatoceles are thought to be the result of pathologic dilation of the efferent ducts.

Testicular histology reveals evidence of both exocrine (sperm production) and endocrine (androgen production) functions within the organ. In the normal, adult testis, seminiferous tubules are lined with a basement layer of laminated connective tissue containing elastic fibers and flattened myoid cells. On this layer rests the germinal epithelium and sustentacular cells known as Sertoli cells. The intertubular connective tissue contains groups of large polygonal cells termed Leydig cells, whose cytoplasm holds many lipid granules that contain testosterone and other androgens. Characteristics of maleness, including body hair, muscle mass, deepened voice, and sexual function are several androgen-dependent functions.

The epididymis is a comma-shaped organ located along the posterolateral surface of the testis. It is a tightly coiled, tortuous duct 3 to 4 m in length, embedded in dense connective tissue. Passage through the epididymis induces many changes to newly formed sperm, including a gain in functional motility and alterations in surface charge, membrane proteins, immunoreactivity, phospholipids, fatty acid content, and adenylate cyclase activity. These changes improve cell membrane structural integrity, increase fertilization ability, and improve motility. Spermatozoa within the testis have very poor or no motility. They become progressively motile and functional only after traversing the epididymis. The transit time of sperm through the epididymis has been estimated at 12 days in humans.

Extensions from the tunical sheath that surrounds the epididymis enter interductal spaces and form septa that divide the duct into histologically characteristic regions: the caput or head, corpus or body, and cauda or tail. The 8 to 10 ductuli efferentes within the caput region coalesce to form a single epididymal duct within the corpus and cauda epididymis. The epididymis is distinguished histologically by its ciliated epithelium that consists of two main cell types: principal cells and basal cells. Principal cells vary in height along the length of the epididymis mainly because of the length of associated stereocilia. Principal cell nuclei are elongated and often possess large clefts and one or two nucleoli. Consistent with absorptive and secretory function, their cellular apices have numerous coated pits. There are far fewer basal cells than principal cells in the epididymis. Tear-shaped basal cells rest on the basal lamina and extend approximately toward the lumen, their apices forming threads between adjacent principal cells. Thought to be derived from macrophages, they are likely the precursors of the principal cells.

The vas deferens originates as a continuation of the cauda epididymal duct. During this transition, the muscular coat of the tubule increases dramatically, the tortuosity of the duct decreases, and epithelial cells lose cilia. The vas continues for about 25 cm and becomes the ampulla of the vas before joining with the seminal vesicle and forming the proximal ejaculatory duct. In cross section, the vas deferens has an outer adventitial connective tissue sheath containing blood vessels and small nerves, a muscular coat that consists of a middle circular layer surrounded by inner and outer longitudinal muscle layers, and an inner mucosal layer with a pseudostratified epithelial lining. The outer diameter of the vas deferens varies from 1.5 to 3 mm, and the lumen of the unobstructed vas deferens varies from 0.2 to 0.7 mm in diameter, dimensions easily handled using microsurgical approaches to surgical reconstruction after vasectomy or other blockage.

TESTICULAR DEVELOPMENT AND SPERMATOGENESIS

Histologically, newborn testes appear as “testis cords” that harbor mainly Sertoli cells and rarer early germ cells, called gonocytes, in layers without tubular lumina. Consistent with a brief surge in androgen levels during the first few months of life that is thought to hormonally imprint later androgen-dependent organs, large prominent interstitial Leydig cells occupy the spaces among the testis cords. In early childhood, little change occurs in the testis cords except for linear growth. At 5 to 7 years of age, lumina begin to appear in the cords and they gradually increase in diameter to become seminiferous tubules, characterized by primitive spermatogonial stem cells and marking the first stage of spermatogenesis. Mitotic activity of early spermatogonia begins at about 11 years of age; however, the age at which the germ cells begin to differentiate varies greatly, as does the onset of puberty. Primary spermatocytes appear soon thereafter, indicating the beginning of meiosis in the testis, and spermatids are noted at about 12 years of age. Once this germ cell maturation sequence (termed spermarche ) begins, the testes enlarge rapidly and constitute one of the first signs of puberty (Tanner stage I).

The interstitial Leydig cells mature concurrently with germ cells during early puberty, but androgen production lags slightly behind spermatogenesis. The pubertal surge in testosterone from mature Leydig cells is responsible for the remainder of pubertal development (Tanner stages II to V). Spermatogenesis remains active throughout adult life but decreases during the seventh or eighth decade with the onset of andropause, as a response to decreased androgen production by Leydig cells.

Spermatogenesis is a continuous process in vertebrates (only seasonal in some moose species) and, in males, involves germ cell progression though 13 cell types over a period of 64 days. It consists of (1) a proliferative phase as spermatogonia divide to replace their number (self-renewal) or differentiate into daughter cells that become mature gametes; (2) a meiotic phase when germ cells undergo a reduction division, resulting in haploid (half the normal DNA complement) spermatids; and (3) a spermiogenesis phase in which spermatids undergo a profound metamorphosis to become mature sperm.

Spermatogenesis begins with type B spermatogonia dividing mitotically to form primary spermatocytes within the adluminal compartment. Primary spermatocytes are the first germ cells to undergo meiosis. As they move from the adluminal or basal to luminal or apical compartment of the Sertoli cell (as defined by intercellular tight junctions), they divide into secondary spermatocytes. The latter cleave immediately into spermatids, which metamorphose into mature sperm.

A cycle of spermatogenesis involves the division of spermatogonial stem cells into sperm. Several cycles of spermatogenesis coexist within the germinal epithelium at any one time and are described morphologically as stages. When viewed from a fixed point within a seminiferous tubule, six recognizable stages exist in humans. Superimposed on this, there is also a specific organization of spermatogenic cycles within the seminiferous tubule space, termed spermatogenic waves. It is likely that human spermatogenesis occurs in a spiral or helical wave pattern that ensures constant and not pulsatile sperm production at 1200 sperms/heartbeat.

There are two important differences between mitosis and meiosis. During the phase of DNA synthesis in both mitosis and meiosis, reproducing cells have double the normal content of DNA (4 n ). In mitosis, DNA content is reduced to diploid (2n) after a single reduction division. However in meiosis, a second reduction division (secondary spermatocytes to spermatids) occurs to generate daughter cells with haploid ( n ) DNA content consisting of 22 autosomes and either an X or a Y chromosome. The other difference is that mitosis produces identical daughter cells, whereas genetically different daughter cells result from meiosis. This occurs as a consequence of chromosomal synapse and recombination during meiosis, in which DNA is exchanged between sister chromatids and is the basis for genetic diversity in our species.

DESCENT OF THE TESTIS

The early genital ridge on the posterior wall of the coelomic cavity contains the primordial testis and extends from the sixth thoracic to the second sacral segment. At 8 weeks' gestation, the testis, lying beneath the mesothelium (primitive peritoneum), becomes an elongated, spindle-shaped organ projecting into the coelomic cavity (future abdominal cavity). The mesothelium is thrown into two folds: the upper, diaphragmatic or cranial suspensory ligament extends to the diaphragm, whereas the lower, inguinal ligament or future gubernaculum terminates in the lower abdominal wall at a site where the inguinal bursa (future inguinal canal) is to develop. A pouch-like peritoneal evagination of the abdominal wall, termed the processus vaginalis, emerges during the sixth month. It grows to become the inguinal bursa, which, by the end of the seventh month is large enough to admit the testis. Concurrently, as a result of an involution of the cranial and adjacent mesonephros, the testis becomes mobile and is left suspended from the epididymis by the mesorchium, a fold of primitive peritoneum. By 7 months, the gonad is located several millimeters above the groin, with its long axis oriented obliquely or at right angles to the embryo.

At the end of the seventh month, the testes pass inferiorly through the inguinal canal. However, it is not uncommon to find them in the canal at birth, with final descent occurring postnatally. At the time of testis descent into the processus vaginalis within the inguinal bursa and scrotum, the portion of this processus vaginalis superior to the testis becomes obliterated sometimes weeks or months after birth. Persistence of the processus vaginalis after birth can result in what is called a communicating hydrocele, in which peritoneal fluid freely enters the tunical vaginalis space within the scrotum. This type of hydrocele is characterized by dramatic changes in size when assuming an upright or supine position.

The gubernaculum, originally discernible as a fibrous band in early fetal life, develops as the lower inguinal ligament and increases in size through the seventh month of gestation. It connects the upper end of the wolffian duct (epididymis), and with it the testis, to the lower abdominal wall. The distal attachment of the gubernaculum extends to the region of the inguinal bursa where the future external oblique layer of the abdominal wall develops.

The role of the gubernaculum in the descent of the testis is incompletely understood. What is known is that testis descent occurs in two stages: transabdominal migration and inguinoscrotal descent. Failure of either stage results in varying degrees in what is termed undescended testis or cryptorchidism. Initially, the gubernaculum contracts and thickens to guide migration of the testis toward the internal inguinal ring. In mice, this migration appears to be controlled by a testis-derived insulin-like/relaxin-like peptide (Insl-3). The human homologue of the mouse Insl3 gene has been identified as an insulin and relaxin-like molecule ( INSL3 ) and is produced by Leydig cells. In studies of cryptorchid boys, mutations in the INSL3 gene only occur in 1% to 2% of cases, suggesting that other factors must also play a role in testis descent. The second phase of descent, transinguinal to scrotal, is thought to be androgen dependent. This is surmised from conditions such as androgen insensitivity (faulty androgen receptor activity) and Kallmann syndrome (defective androgen production) in which there is transabdominal but not inguinoscrotal descent observed. It also follows that endocrine disruptors that alter androgen balance in the third fetal trimester may also predispose male infants to cryptorchidism.

SCROTAL SKIN DISEASES I: CHEMICAL AND INFECTIOUS

Many skin diseases of infectious, allergic, or metabolic origin can involve the scrotum. Among many yeasts, molds, and fungi, only a few are infectious and are termed dermatophytes (“skin fungi”). Skin fungi live only on the dead layer of keratin protein on the skin surface. They rarely invade deeper and cannot live on mucous membranes. Infections by the fungus tinea cruris (ringworm) are very common in the groin and scrotum. It involves desquamation of the scrotal skin and contiguous surfaces of the inner thighs and itches (“jock itch”). Tinea begins with fused, superficial, reddish-brown, well-defined scaly patches, which extend and coalesce into large, symmetrical, inflamed areas. The margins of the lesions are characteristically distinct. The initial lesion may become macerated and infected and is painful and itches. Sweating, tight clothing or obesity favor development and recurrence of this fungal infection, derived mainly from the genera Trichophyton and Microsporum . These same organisms cause tinea pedis or “athlete's foot.”

Contact dermatitis (dermatitis venenata) is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the superficial regions of the skin are affected, including the epidermis and the outer dermis. Unlike contact urticaria, in which a rash appears within minutes of exposure and fades away within minutes to hours, contact dermatitis takes days to fade away. The most common causes of allergic contact dermatitis are poison ivy, poison oak, and poison sumac. Common causes of irritant contact dermatitis are highly alkaline soaps, detergents, and cleaning products. Contact dermatitis of the scrotum may show a variety of lesions varying from erythema, to papules, to vesicles or pustules, but is always accompanied by itching. The scrotal skin is usually swollen, occasionally edematous, painful, and red. Treatment is directed toward discovery and elimination of the specific cause. Drug eruption is a form of contact dermatitis that may occur on the scrotum and elsewhere on the body after consumption of drugs to which the patient is allergic.

Allergic eczema or atopic dermatitis often occurs together with other atopic diseases like hay fever, asthma, and conjunctivitis. It is a familial and chronic disease and can appear or disappear over time. Atopic dermatitis can often be confused with psoriasis. It usually begins with superficial excoriation, localized edema, and exudation, following which the lesion progresses to dry, thickened skin with scale formation and a brownish hue. Marked pruritus or itching and pustule formation are characteristic. The underlying cause remains obscure. Herpes simplex virus type II (HSV-2, see Plate 2-21 ) is a form of genital herpes located on the genitals that is more commonly observed on the penis than the scrotum.

Intertrigo or thrush is an erythematous, inflammatory condition occurring where contiguous skin surfaces are moist and warm. It is caused by the yeast Candida albicans that is normally found on the skin. It is usually symmetrical on the scrotum and inner surfaces of the thighs, with frequent involvement of the penis and buttocks. Abrasions may lead to fissures and maceration, with the skin becoming secondarily infected with bacteria. If the diagnosis is in doubt, a KOH test can be performed to detect the candidal yeast. A bacterial culture can help diagnose a secondary bacterial infection. Intertrigo is treated with antifungal creams such as clotrimazole and miconazole. Equally important is to keep the skin folds as dry as possible.

Other rare skin lesions (not illustrated) with a predilection for the scrotum are prurigo, which is a general term for itchy eruptions of the scrotal skin, and lichen planus, an inflammatory skin rash that forms scaly rings and plaques on the genitalia that are characteristically “violaceous” or purple colored. Erythrasma of the genital region, a chronic infection by the bacteria Corynebacterium minutissimum , appears as a brown, scaly, finely demarcated eruption that produces no symptoms. Tinea versicolor, caused by the fungus Pityrosporum ovale , is relatively common in adolescent and young adult males. It appears as enlarging brown macules without inflammation or other symptoms and is treated with typical antifungal creams.

SCROTAL SKIN DISEASES II: SCABIES AND LICE

Scabies is a contagious, parasitic skin disorder caused by the mite Sarcoptes scabiei . Mites are small, eight-legged parasites (in contrast to six-legged insects), 1/3 mm long, that burrow into the skin and that are especially active at night, producing intense nocturnal itching. Furrows are readily visible on the scrotum, and a tiny burrow can be detected at the point where the skin has been invaded. The furrows vary in length and coloration and are usually curved or arciform, resembling a small beaded or dotted thread. At the distal, closed end of the tortuous channel, a small vesicle develops where the mite is lodged. Scraping the vesicle usually produces the mite and eggs that can be visualized in 10% NaOH solution. The vesicles quickly transform into papules, pustules, incrustations, and excoriations that obscure the burrows. Once secondary excoriation and pustules develop, the original skin lesions are more difficult to recognize. In children, scabies is frequently complicated by impetigo of the buttocks. Skin-to-skin contact is the most common mode of spread and human scabies is not obtained from animal contact. Scabies is curable with permethrin, crotamiton, or lindane creams.

Pediculosis pubis is a result of infestation by the crab louse ( Pthirus pubis ). This ectoparasite feeds exclusively on blood and has an oral appendage that produces a skin lesion by suction. Unlike the body louse that lives in clothing, the crab louse resides on hairy body parts: in the genitalia, this louse attaches to pubic hair with its head buried in the hair follicle. Usually acquired during sexual contact, these lice rarely produce large skin lesions, and most commonly cause scratching. Because these organisms are most often spread through close or intimate contact, pediculosis is classified as a sexually transmitted disease (STD) that is not prevented with condom use. The skin may reveal a “bitten” appearance, showing small red points that may develop into papules. Scratching leads to excoriation, bleeding, and incrustation and a brownish discoloration of the skin. In addition, blue spots or macula cerulea up to 0.5 cm in diameter can occur on the skin as a result of the bite of the louse and is likely a consequence of a reaction between the louse saliva and the host blood. These blue spots do not disappear under pressure and are characteristic of pediculosis.

A careful search among the pubic hairs for nits, nymphs, and adults should be made in cases of pruritus. Lice and nits can be removed either with forceps or by cutting the infested hair with scissors and then examined with a microscope. Crab lice are also treated and killed with permethrin or lindane creams. A second treatment is recommended 10 days after the first. It is also crucial that all bed linens be changed and put into well-sealed plastic bags for 2 weeks before washing to destroy the lice eggs that may be a source of reinfestation.

AVULSION, EDEMA, HEMATOMA

Traumatic avulsion of the scrotum and penis is seen with animal attacks, motor vehicle accidents, assaults with sharp or high-velocity missiles, self-mutilation, and machinery-related (i.e., industrial, agricultural) accidents. It is most commonly observed in men aged 10 to 30 years. The entire scrotal tissue may be lost and complete sloughing of remaining skin may occur due to infection. Partial loss of the scrotum is managed by debridement, excision of islands of remnant full-thickness scrotal wall, and primary closure with absorbable sutures. If the complete scrotal skin has been avulsed, it may be necessary to transplant the uninjured testes into the subcutaneous tissues of the upper thigh or within the inguinal region. The ability of small fragments of remaining skin to regenerate a full-sized scrotum is remarkable, and transplantation of the testes can be avoided if some skin remains. The vascularity, compliance, and elasticity of the dartos layer allow scrotal flaps to cover substantial areas of loss. Clean granulation tissue usually coats the surface of the exposed testicles, followed by regeneration of the scrotum.

Complete scrotal loss requires skin grafting to expedite healing. Split-thickness grafting (0.008 to 0.014 in) that is meshed to allow fluid to drain is ideal for scrotal coverage because it does not result in hair growth. With the penis, split-thickness skin grafts are needed for the denuded area, as the penile skin must be pliable to allow for erections. Healing by regeneration of skin from a nearby avulsed margin would result in a relatively inelastic covering. Testicles should be fixed together in a dependent position to minimize motion and maximize graft “take.” The use of “thigh pouches” for the testes may be necessary with infected wounds until they are clean enough for grafting. Long-term success with skin grafting for scrotal injury is excellent. Only 20% of patients require significant revisions and most of these can be managed in the office. Acute trauma without infection can be managed simply with wet-to-dry dressings until definitive graft placement.

Edema of the scrotum results from either localized or generalized pathology. The loose and elastic structure of the scrotum facilitates edema from even the slightest inflammatory reaction or vascular or lymphatic disturbance. Epididymo-orchitis is frequently accompanied by scrotal edema, as are allergic states or obstruction of the lymphatic or vascular system. Marked edema or anasarca that involves the scrotum can result from chronic cardiac insufficiency, liver cirrhosis, ascites, and renal failure. Malignancy affecting retroperitoneal and inguinal lymph nodes may, by obstructing the lymphatics, result in a nonpitting edema of the scrotum. Simple edema may also be the first sign of elephantiasis (lymphatic filariasis) and other tropical diseases. Trauma or surgery to the scrotum is usually followed by a considerable amount of edema. Notable edema may also result from spider bites or allergies (angioneurotic edema). When the edema is massive, the dependent portion of the scrotal skin may become moist, denude, and form ulcers. Patients with scrotal edema should elevate the scrotum to accelerate venous and lymphatic drainage.

Scrotal hematoma or diffusion of blood through the subcutaneous scrotal tissue is most commonly observed after scrotal surgery or blunt trauma. The scrotum is an uncommon location for idiopathic bleeding, as its contracting smooth muscle layers efficiently compress blood vessels. With an acute bleed, the scrotum becomes dark and assumes a purple color. Over time, the coloration changes to yellow and then to normal color. However, it may take several weeks for blood pigments to be resorbed and for normal skin color to be completely restored. Hematoma is usually accompanied by variable degrees of edema and should be treated with moderate compression, suspension, and the application of ice or cold packs as early as possible. If bleeding is brisk, it may extend upward into the inguinal area and frequently over the penis under the continuity of the dartos and Scarpa and Colles fasciae (see Plate 2-20 ).